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Ultrastructural changes induced by experimental subarachnoid haemorrhage and 6-hydroxydopamine in cat cerebral
F Rivilla1, J Marín, C F Sánchez-Ferrer
1Department of Pharmacology and Therapeutics, School of Medicine, Autonomous University, Madrid, Spain.
Insights
Subarachnoid bleeding causes damage to cerebral arteries, including denervation, which may lead to cerebrovascular spasm. Other mechanisms beyond denervation also contribute to vasospasm.
Area of Science:
- Neuroscience
- Vascular Biology
- Pathology
Background:
- Cerebrovascular spasm is a serious complication following subarachnoid hemorrhage.
- The precise mechanisms underlying vasospasm remain incompletely understood.
Purpose of the Study:
- To investigate the ultrastructural changes in cerebral arteries after subarachnoid hemorrhage.
- To explore the role of denervation in the pathophysiology of vasospasm.
Main Methods:
- Transmission electron microscopy was used to examine the middle cerebral artery of cats.
- Cats were subjected to subarachnoid blood injection and observed at 3 and 7 days post-injection.
- The effects of 6-hydroxy-dopamine (6-OHDA) on cerebral vessels were also assessed.
Main Results:
- Subarachnoid hemorrhage induced significant ultrastructural damage to the intima, media, and adventitia of cerebral arteries.
- Endothelial cells showed swelling and vacuolization, with disrupted tight junctions.
- Adventitial changes included axonal swelling and loss of synaptic vesicles, indicating denervation.
- 6-OHDA administration caused similar adventitial changes, suggesting denervation contributes to vasospasm.
- However, subarachnoid hemorrhage also affected the intima and tunica media, indicating additional mechanisms are involved.
Conclusions:
- Denervation induced by subarachnoid bleeding is a potential factor in cerebrovascular spasm.
- Mechanisms beyond denervation, affecting the intima and tunica media, also contribute to vasospasm following subarachnoid hemorrhage.
Abstract:
Transmission electron microscopy of the middle cerebral artery from cats exposed to subarachnoid injection of blood 3 and 7 days before, showed several damage of the vascular ultrastructure. The intima was thickened with swelling and vacuolization of endothelial cells, with a plump appearance and disruption of tight junctions. The cellular surface was corrugated and the subendothelial space contained proliferating and vacuolated smooth muscle cells capped by elastin and collagen fibres. The internal elastic lamina was also corrugated and disrupted. The adventitial changes were axonic cytoplasmic and mitochondrial swelling, virtual absence of synaptic vesicles, and disruption of the outer axonal membrane, suggesting denervation of cerebral vessels. With administration of 6-hydroxy-dopamine (6-OHDA), similar ultrastructural changes were observed in the adventitia. These observations indicate that denervation induced by subarachnoid bleeding could be involved in the pathophysiology of cerebrovascular spasm. Subarachnoid haemorrhage, but not 6-OHDA, affects also intima and tunica media, suggesting other mechanisms, in addition to denervation, can participate in the vasospasm.